Depot-specific regulation of NAD+/SIRTs metabolism identified in adipose tissue of mice in response to high-fat diet feeding or calorie restriction

Wei, Xiaojing; Jia, Ru; Wang, Guan; Hong, Shangyu; Song, Lin; Sun, Bo; Chen, Ke; Wang, Nan; Wang, Qiqi; Luo, Xiao; Yan, Jiaqi

doi:10.1016/j.jnutbio.2020.108377

Cited by 18 publications

(17 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, SIRT1 expression is increased in BAT of mice upon a 48-h fast (Cordeiro et al, 2013) and 40% CR (Wei et al, 2020). Genetic over-expression (Boutant et al, 2015) and activation (SIRT1720) (Feige et al, 2008) of SIRT1 in mice induces BAT thermogenesis and lipid catabolism, which are mediated by increased expression of BAT-selective transcriptional regulators (PPARα, PPARγ, PGC-1α, PGC-1β, FOXO1, FOXO3a), uncoupling and detoxification factors (UCP1, UCP3, SOD1, SOD2) and FAO genes (Mcad, Lcad, Cpt1b, Cpt1a) (Feige et al, 2008;Boutant et al, 2015).…”

Section: Class III Hdac (Sirt1)mentioning

confidence: 97%

Understanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases

et al. 2020

View full text Add to dashboard Cite

The global prevalence of metabolic disorders, such as obesity, diabetes and fatty liver disease, is dramatically increasing. Both genetic and environmental factors are wellknown contributors to the development of these diseases and therefore, the study of epigenetics can provide additional mechanistic insight. Dietary interventions, including caloric restriction, intermittent fasting or time-restricted feeding, have shown promising improvements in patients' overall metabolic profiles (i.e., reduced body weight, improved glucose homeostasis), and an increasing number of studies have associated these beneficial effects with epigenetic alterations. In this article, we review epigenetic changes involved in both metabolic diseases and dietary interventions in primary metabolic tissues (i.e., adipose, liver, and pancreas) in hopes of elucidating potential biomarkers and therapeutic targets for disease prevention and treatment.

show abstract

Section: Class III Hdac (Sirt1)mentioning

confidence: 97%

Understanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The most consistent benefit is probably aiding in losing body weight (Liu et al, 2016a;Yamamoto et al, 2016;Cohen et al, 2017;Miller et al, 2017;Waldman et al, 2018;Yu et al, 2018;Wei et al, 2020). The effect is seen in various experimental rodent models.…”

Section: Caloric Restrictionmentioning

confidence: 97%

“…As shown by reducing immune cell infiltration in heart and decreasing toll-like receptor (TLR) 2, TLR4, and TNFα in a diabetic mice model with cardiometabolic phenotypes (Cohen et al, 2017;Waldman et al, 2018). Caloric restriction is also found to reduce the systemic sterile inflammation in a dietinduced obesity mice model, where serum interleukin (IL)-6, and TNFα is lowered (Wei et al, 2020). These recent studies had shown that caloric restriction had their benefits which can be related to the elevation of NAD + or raise in the expression or activities of sirtuins in the target tissue (adipose tissue for obesity, or aortae and heart for CVD).…”

Section: Caloric Restrictionmentioning

confidence: 98%

“…The effect is seen in various experimental rodent models. The underlying mechanism is thought to be related to the raise of SIRT1 expression within the adipose tissue (Miller et al, 2017;Wei et al, 2020), and the elevation of NAD + synthesizing enzyme NAMPT expression and to the fueling of NAD + pool (Miller et al, 2017;Wei et al, 2020) to lose adipose tissue weight and/or reduce the lipid accumulation in adipocytes.…”

Section: Caloric Restrictionmentioning

confidence: 99%

“…A second beneficial effect comprises an improved blood lipid profile. Caloric restriction treatment reduces total cholesterol (Cohen et al, 2017;Waldman et al, 2018), total triglycerides (Liu et al, 2016a;Waldman et al, 2018;Yu et al, 2018;Wei et al, 2020) in blood, and this poses a positive effect on cardiovascular diseases. Interestingly, it is accompanied with the raised expression of sirtuins in heart (Waldman et al, 2018;Yu et al, 2018) or aorta (Liu et al, 2016a) in rodent models, further contributing to the beneficial effects on reducing the risk of cardiovascular diseases.…”

Section: Caloric Restrictionmentioning

confidence: 99%

See 2 more Smart Citations

Modulating Sirtuin Biology and Nicotinamide Adenine Diphosphate Metabolism in Cardiovascular Disease—From Bench to Bedside

et al. 2021

View full text Add to dashboard Cite

Sirtuins (SIRT1–7) comprise a family of highly conserved deacetylases with distribution in different subcellular compartments. Sirtuins deacetylate target proteins depending on one common substrate, nicotinamide adenine diphosphate (NAD+), thus linking their activities to the status of cellular energy metabolism. Sirtuins had been linked to extending life span and confer beneficial effects in a wide array of immune-metabolic and cardiovascular diseases. SIRT1, SIRT3, and SIRT6 have been shown to provide protective effects in various cardiovascular disease models, by decreasing inflammation, improving metabolic profiles or scavenging oxidative stress. Sirtuins may be activated collectively by increasing their co-substrate NAD+. By supplementing NAD+ precursors, NAD+ boosters confer pan-sirtuin activation with protective cardiometabolic effects in the experimental setting: they improve endothelial dysfunction, protect from experimental heart failure, hypertension and decrease progression of liver steatosis. Different precursor molecules were applied ranging from nicotinamide (NAM), nicotinamide mononucleotide (NMN) to nicotinamide riboside (NR). Notably, not all experimental results showed protective effects. Moreover, the results are not as striking in clinical studies as in the controlled experimental setting. Species differences, (lack of) genetic heterogeneity, different metabolic pathways, dosing, administration routes and disease contexts may account for these challenges in clinical translation. At the clinical scale, caloric restriction can reduce the risks of cardiovascular disease and raise NAD+ concentration and sirtuin expression. In addition, antidiabetic drugs such as metformin or SGLT2 inhibitors may confer cardiovascular protection, indirectly via sirtuin activation. Overall, additional mechanistic insight and clinical studies are needed to better understand the beneficial effects of sirtuin activation and NAD+ boosters from bench to bedside.

show abstract

Aldose reductase promotes diet‐induced obesity via induction of senescence in subcutaneous adipose tissue

Thiagarajan

Quadri

Jawahar

et al. 2022

Obesity

View full text Add to dashboard Cite

ObjectiveAldose reductase (AKR1B1 in humans; Akr1b3 in mice), a key enzyme of the polyol pathway, mediates lipid accumulation in the murine heart and liver. The study objective was to explore potential roles for AKR1B1/Akr1b3 in the pathogenesis of obesity and its complications.MethodsThe study employed mice treated with an inhibitor of aldose reductase or mice devoid of Akr1b3 were used to determine their response to a high‐fat diet. The study used subcutaneous adipose tissue‐derived adipocytes to investigate mechanisms by which AKR1B1/Akr1b3 promotes diet‐induced obesity.ResultsIncreased expression of aldose reductase and senescence in the adipose tissue of humans and mice with obesity were demonstrated. Genetic deletion of Akr1b3 or pharmacological blockade of AKRIB3 with zopolrestat reduced high‐fat‐diet‐induced obesity, attenuated markers of adipose tissue senescence, and increased lipolysis.ConclusionsAKR1B1/Akr1b3 modulation of senescence in subcutaneous adipose tissue contributes to aberrant metabolic responses to high‐fat feeding. These data unveil new opportunities to target these pathways to combat obesity.

show abstract

Depot-specific regulation of NAD+/SIRTs metabolism identified in adipose tissue of mice in response to high-fat diet feeding or calorie restriction

Cited by 18 publications

References 41 publications

Understanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases

Understanding Dietary Intervention-Mediated Epigenetic Modifications in Metabolic Diseases

Modulating Sirtuin Biology and Nicotinamide Adenine Diphosphate Metabolism in Cardiovascular Disease—From Bench to Bedside

Aldose reductase promotes diet‐induced obesity via induction of senescence in subcutaneous adipose tissue

Contact Info

Product

Resources

About